Neuroscientists have discovered brain circuitry for encoding positive and negative learned associations in mice. After finding that two circuits showed opposite activity following fear and reward learning, the researchers proved that this divergent activity causes either avoidance or reward-driven behaviors. Funded by the National Institutes of Health, they used cutting-edge optical-genetic tools to pinpoint these mechanisms critical to survival, which are also implicated in mental illness.
“This study exemplifies the power of new molecular tools that can push and pull on the same circuit to see what drives behavior,” explained Thomas R. Insel, M.D., director of NIH’s National Institute of Mental Health (NIMH). “Improved understanding of how such emotional memory works holds promise for solving mysteries of brain circuit disorders in which these mechanisms are disrupted.”
NIMH grantee Kay Tye, Ph.D. External Web Site Policy, Praneeth Namburi and Anna Beyeler, Ph.D., of the Massachusetts Institute of Technology (MIT), Cambridge, and colleagues, report their findings April 29, 2015 in the journal Nature.
Prior to the new study, scientists suspected involvement of the circuits ultimately implicated, but were stumped by a seeming paradox. A crossroads of convergent circuits in an emotion hub deep in the brain, thebasolateral amygdala, seem to be involved in both fear and reward learning, but how one brain region could orchestrate such opposing behaviors – approach and avoidance – remained an enigma. How might signals find the appropriate path to follow at this fork in the road?

By Rachel E. Gross
“By being a guy’s best first move … Axe is designed to keep guys a step ahead in the dating game,” boasts Unilever, the company that sells Axe products. Of course, if you don’t happen to be a gullible 13-year-old boy, you probably don’t believe that body spray or deodorant is a magic elixir with the power to turn nice girls naughty. But what if it were possible to change a person’s mood with just a scent? The idea may not be that far-fetched, according to a new study in the journal Psychological Science—reporting work that was funded by Unilever. The study found that it might be possible to subconsciously trigger a state of happiness using the scent of—deep breath now—human sweat.
People send all kinds of secret messages through their secretions. When smelling chemicals in male sweat, women become more alert, and they can even tell whether that sweat was made by a guy who was particularly turned on. (Cautions the New York Times: “No man should imagine that based on these conclusions he can improve his sex life by refraining from bathing.”) But until now, most sweat studies have focused on sexual arousal or negative emotions like fear. For obvious reasons, these emotions are crucial to survival and evolutionary success. If your friend spots a puma, it may be helpful for you to be able to sniff out instant cues to be on the alert or flee for cover.
Being able to transmit positive emotions may also have a profound social impact, says Gün Semin, a psychologist at Utrecht University in the Netherlands and lead researcher on the study. After all, “the pursuit of happiness is not an individual enterprise,” as he and his fellow researchers write rather eloquently in the new study. So Semin’s team decided to test whether people could communicate happiness via sweat.

Two drugs already on the market — an antifungal and a steroid — may potentially take on new roles as treatments for multiple sclerosis. According to a study published in Nature today, researchers discovered that these drugs may activate stem cells in the brain to stimulate myelin producing cells and repair white matter, which is damaged in multiple sclerosis. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.
Specialized cells called oligodendrocytes lay down multiple layers of a fatty white substance known as myelin around axons, the long “wires” that connect brain cells. Myelin acts as an insulator and enables fast communication between brain cells. In multiple sclerosis there is breakdown of myelin and this deterioration leads to muscle weakness, numbness and problems with vision, coordination and balance.
“To replace damaged cells, the scientific field has focused on direct transplantation of stem cell-derived tissues for regenerative medicine, and that approach is likely to provide enormous benefit down the road. We asked if we could find a faster and less invasive approach by using drugs to activate native nervous system stem cells and direct them to form new myelin. Our ultimate goal was to enhance the body’s ability to repair itself,” said Paul J. Tesar, Ph.D., associate professor at Case Western Reserve School of Medicine in Cleveland, and senior author of the study.
It is unknown how myelin-producing cells are damaged, but research suggests they may be targeted by malfunctioning immune cells and that multiple sclerosis may start as an autoimmune disorder. Current therapies for multiple sclerosis include anti-inflammatory drugs, which help prevent the episodic relapses common in multiple sclerosis, but are less effective at preventing long-term disability. Scientists believe that therapies that promote myelin repair might improve neurologic disability in people with multiple sclerosis.

By Sandra G. Boodman A
Braced by her partner, Suzanne Tobin shuffled back to her car parked in the cavernous garage at Johns Hopkins Hospital late on the evening of Oct. 22, 2013, distraught about what might happen next.
Tobin, then 60, had been driven by her partner, James Rapp, from their Germantown home to the Hopkins ER in hopes that doctors there could determine what was causing her relentless deterioration. Three months earlier, Tobin had held a full-time job as a copy editor at AARP in the District. She spent an hour before work striding around the Mall for exercise. Now she could no longer walk unassisted, her speech was nearly unintelligible and her left hand was so weak she could no longer hold a book.
Doctors in suburban Maryland had diagnosed a stroke — or possibly a series of strokes — but were unable to explain why Tobin kept getting worse by the week. Her neurologist counseled patience and offered to prescribe antidepressants, drugs that Tobin had told him she had taken for years.
An occupational therapist she’d been seeing had expressed alarm; stroke patients tended to plateau or even improve over time, not to experience a steady downward spiral. “You need to get a new neurologist,” she advised Tobin.
Tobin and Rapp decided their best bet was to head to Hopkins in Baltimore. But after 12 hours and a battery of tests, including a CT, MRI and other scans, emergency physicians sent Tobin home. They found no new stroke — an earlier MRI that Rapp had brought along appeared to show an old one — nor any other problem that would require immediate hospitalization. They advised her to follow up with her regular doctors.